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2c-t-7 toxicity

H

HeaT

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I've become captivated by 2c-t-7's power, and been reading a lot about it lately. It seems that much lower doses insufflated can be lethal, and MDMA increases the toxicity a lot (with high doses of 2c-t-7). I've also read that becoming violent is a sign of overdose, and 2 of the 3 reported fatalities were extremely violent and angry before death, in fact one screamed "I DONT WANT TO DIE, FUCK THIS" or something to that effect before dying.

Anyone have any clue as to why 2c-t-7 is like this? Lethal doses have been only twice what a "strong" dose of 2c-t-7 is insufflated, and less than a strong dose orally.

I really want to try this chemical, because like I stated earlier, I'm amazed by it, but at the same time, the deaths and thin line between a strong and lethal dose (or overdose).
 
2CT7 has quite a unique mixture of effects; it is

(i) a 5HT2A agonist
(ii) a serotonin releaser
(iii) a potent and selective MAO-A inhibitor

Now of these its the MAOI action that you need to be concerned about when thinking of potential toxicity. Combining a MAOI with stimulants or serotonin releasers is dangerous normally, so when you have serotonin release and MAO-A inhibition occuring from the same compound then there is an obvious risk of serotonin syndrome especially at higher doses.

If you read the case reports for the deaths, one of them was from 2CT7 + MDMA + ephedrine, and another was from 2CT7 + MDMA, only one was from 2CT7 alone and if i remember correctly the cause of death in that case was aspiration of vomit rather than malignant hyperthermia or status epilepticus.

So 2CT7 is mainly dangerous when taken in large doses (30mg or more) or when combined with drugs like ephedrine or MDMA which aren't safe to take with MAOIs in the first place. That said, the first time i tried 2CT7 i took it with MDMA and 5HTP and i didn't die or suffer any adverse reaction...but i guess its dose-dependant, i only had 1/2 a 2CT7 pill with 1/2 an ecstasy pill, if id taken two whole pills of each then maybe i wouldn't be sitting here writing this...
 
Some users have recently reported either taking themselves to the hospital or being taken to the emergency room from 2C-T-7 alone. Users who have taken as little as 10mg orally have reported being overwhelmed with anxiety and discomfort, while some users who have snorted 15mg or taken 30mg or more orally report being completely overwhelmed by the intensity of the experience
Dosage
Threshold 3 - 5 mg
it is dangerous for first time users to snort more than a few milligrams because people have had dissociated, overwhelming experiences on as little as 6mg insufflated
I also recommend a very accurate scale to weigh the doses out
 
mad_scientist said:
2CT7 has quite a unique mixture of effects; it is

(i) a 5HT2A agonist
(ii) a serotonin releaser
(iii) a potent and selective MAO-A inhibitor
Click to expand...

Are there any published studies about your claims?

2C-T-7 used to be my favourite drug a few years ago. I used to take 15-30mg orally before going to bars with my friends.
 
Well, 2c-t-7 being a MAOI definitely clears that up a lot. Thanks guys. And I have a legit source, don't worry.
 
Yeah I seem to remember some talk about that, but I didn't remember it being about 2C-T-7 specifically, I thought it was related to other, higher homologues...some with whole new rings attached to the 4-thio. So to describe 2C-T-7 as a "potent MAOI" has got me questioning....can you show the source for this? How potent is potent...like harmaline potent? Because all psychedelics have some MAOI action in that they tie up MAO as that system breaks the molecule down.
 
Gallardo-Godoy, A; Fierro A, McLean TH, Castillo M, Cassels BK, Reyes-Parada M, Nichols DE. (April 7, 2005). "Sulfur-substituted alpha-alkyl phenethylamines as selective and reversible MAO-A inhibitors: biological activities, CoMFA analysis, and active site modeling.". Journal of Medicinal Chemistry 48 (7): 2407-19.


They tested a whole bunch of them, including some that weren't in PIHKAL but out of the lot the strongest MAO-A inhibitor was the 4-(n)-propylthio analogue, 2CT7. So its quite likely that all of the 2CT series will be MAO inhibitors, but because 2CT7 is the most potent at doing this, its the most likely that MAO inhibition will be a clinically relevant effect at normal doses.

This is supported especially by the case reports from the deaths, the fact that MDMA coadministration was involved in two of them makes MAO inhibition from the 2CT7 + stimulant / serotonin release --> consequent fatal serotonin syndrome a likely cause of death.
 
Thanks. I need to organize my library as I had this paper. So to those who know about this more than I do....are the MAO properties of T7 significant (like that of harmaline) or not too significant (like that of a-MT and a-ET)?
 
As far as I can remember that paper, it was 2C-T-2 that was the potent MAO-I. I always get it wrong when I try and name chemicals from those structure tables, so the chemicals that look like they would be relatively strong MAOIs are 22a, 22b, 29, 30, 32, 33 and 37 (that is if you need more than roughly 10mg).
 
^^ that's what I thought too from the article, the only thing that confuses me is why 2c-t-7 would drop many more bodies before 2c-t-2. i guess the mechanism that leads to fatality is still somewhat of a mystery. I wish the study would have included more information on non-alpha-alkylated compounds, but at least it provides the synth for the psi-2-c-ts.
 
Hmm well now that i re-read that paper it doesn't look like 2CT7 is even in there, all of those compounds have R7= CH3 or CH2CH3 which means they are the amphetamine analogues, not the phenethylamines.

From Table 1 it looks like the two strongest MAO-A inhibitors are compounds #22b and #29, these being 2,6-dimethoxy-4-ethylthioamphetamine (so psi-ALEPH-2 if we extend Shulgins naming system) and 2,4-dimethoxy-6-chloroamphetamine.

So i was mistaken, there is no evidence from this paper showing whether 2CT7 is an MAO-A inhibitor, or how strongly it might produce this effect. However id say its pretty clear that many structurally related compounds are MAOIs, and i would still cite this as a likely cause for those deaths given that MDMA and/or other stimulants were involved in two of the cases.

EDIT:

Ah yes,

As reported in a previous study of similar compounds as MAO-A inhibitors, potency was a function
of the length of the carbon chain attached to the sulfur at the para position, as indicated by the green contours in Figure 2B, reaching a maximum with a linear three-carbon chain
Click to expand...

So the referance i should have given for 2CT7's MAO inhibition was their #11 from this paper;

Scorza, M. C.; Carrau, C.; Silveira, R.; Zapata-Torres, G.; Cassels,
B. K.; Reyes-Parada, M. Monoamine oxidase inhibitory properties
of some methoxylated and alkylthio amphetamine derivatives:
structure-activity relationships. Biochem. Pharmacol.
1997, 54, 1361-1369.

Thought id seen actual numbers for 2CT7 somewhere!
 
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so a combo of t7 and yohimbe would be bad?
i have used t7 a few times and am keen to use it again
 
So we could do with making something that binds to HT2B receptors more (am I right, thats the trippy one?) but is less of an MAO inhibitor? Don't forget that MTA killed quite a few people without other drugs in their systems. Maybe that X-S-CH2-CH2-SF5 idea might be worth looking into? Maybe combined with the dragonfly? I dunno, just rambling here...
 
So we have reports of serious problems on 2c-t-7, as well as warning signs of when things are going down the tubes (extreme disorientation, violence and agitation, etc).

But is there anything that can be done about it? If a friend on 2c-t-7 were to start running around and screaming, and I called 911, could they do anything to prevent death/toxicity? Would sedatives and/or antipsychotics be helpful? Is there an "MAOI-I" that can counteract its effects?
 
Ideally you would restrain them and then administer IV/IM benzodiazepines and IV saline (especially if there is vomitting) keeping close attention to their BP and heart rate. This is probably what the hospital would do, too. If they're going to die/become comatose, it will happen within 4-5 hours of administering the drug orally, 1 hour nasally, or 5-20 minutes IM most likely.
 
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for a t7 overdose, the best method of control would be to induce coma/sedation (via benzos/sedatives) and put them on a ventilator (pretty much let a machine take over their bodily functions)
 
MAOI PEA/AMP compounds such as PMA and 2CT7 have no place to be done by sane, non-self destructive individuals. What, exactly, is the allure here? Their highs don't even sound that good, really.
 
haribo1 said:
So we could do with making something that binds to HT2B receptors more (am I right, thats the trippy one?) but is less of an MAO inhibitor? Don't forget that MTA killed quite a few people without other drugs in their systems. Maybe that X-S-CH2-CH2-SF5 idea might be worth looking into? Maybe combined with the dragonfly? I dunno, just rambling here...
Click to expand...

5-HT2A is the one responsible for serotonergic hallucinogens. I did find an interesting article that cites 5-HT1B as the culprit for acute cardiovascular effects, so perhaps MAOI is not the problem. Here it is:

5-hydroxytryptamine receptors in the human cardiovascular system.
Kaumann AJ, Levy FO.

The human cardiovascular system is exposed to plasma 5-hydroxytryptamine (5-HT, serotonin), usually released from platelets. 5-HT can produce harmful acute and chronic effects. The acute cardiac effects of 5-HT consist of tachycardia (preceded on occasion by a brief reflex bradycardia), increased atrial contractility and production of atrial arrhythmias. Acute inotropic, lusitropic and arrhythmic effects of 5-HT on human ventricle become conspicuous after inhibition of phosphodiesterase (PDE) activity. Human cardiostimulation is mediated through 5-HT4 receptors. Atrial and ventricular PDE3 activity exerts a protective role against potentially harmful cardiostimulation. Chronic exposure to high levels of 5-HT (from metastatic carcinoid tumours), the anorectic drug fenfluramine and its metabolites, as well as the ecstasy drug 3,4-methylenedioxymethamphetamine (MDMA) and its metabolite 3,4-methylenedioxyamphetamine (MDA) are associated with proliferative disease and thickening of cardiac valves, mediated through 5-HT2B receptors. 5-HT2B receptors have an obligatory physiological role in murine cardiac embryology but whether this happens in humans requires research. Congenital heart block (CHB) is, on occasion, associated with autoantibodies against 5-HT4 receptors. Acute vascular constriction by 5-HT is usually shared by 5-HT1B and 5-HT2A receptors, except in intracranial arteries which constrict only through 5-HT1B receptors. Both 5-HT1B and 5-HT2A receptors can mediate coronary artery spasm but only 5-HT1B receptors appear involved in coronary spasm of patients treated with triptans or with Prinzmetal angina. 5-HT2A receptors constrict the portal venous system including oesophageal collaterals in cirrhosis. Chronic exposure to 5-HT can contribute to pulmonary hypertension through activation of constrictor 5-HT1B receptors and proliferative 5-HT2B receptors, and possibly through direct intracellular effects.
Click to expand...
 
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